the real cause of obesity

[Guest guest]

despite the captions, " healthy, happy and heavy " , and words like, " readers dive,

hike and climb out of obesity stereotypes " i'm not convinced by this article.

if someone wants to be this active in sports, why have extra weight to carry

around? and the second part, where they talk about a rare case of a child

that needed a hormone shot to curb his appetite does not convince me that

the average person is like the unusual child. it reminds me that family

members would explain that in my family we were all overweight because

we had fat cells in our bodies genetically predisposed for us to be

overweight. they told us this as if we were doomed to a life of being

overweight because at cellular level we were different. the biggest

bunk in this article is, quote: " In fact, it is not even clear whether

there are enduring health benefits to weight loss among

obese individuals who do not suffer from diabetes, heart

disease, hypertension, or liver disease. " Please! i heard that from

my siblings so many times. and some of them are paying dearly in

their health for listening to such bunk. this article infuriates me.

http://www.newsweek.com/id/215115?GT1=43002

The Real Cause of Obesity

It's not gluttony. It's genetics. Why our moralizing misses the point.

NEWSWEEK readers dive, hike and climb out of obesity stereotypes

By Friedman | Newsweek Web Exclusive

Sep 10, 2009 | Updated: 9:11 a.m. ET Sep 10, 2009

Despite receiving a MacArthur genius award for her work in Alabama " forging an

inspiring model of compassionate and effective medical care in one of the most

underserved regions of the United States, " Regina 's qualifications to

be surgeon general have been questioned. Why? She is overweight. " It tends

to undermine her credibility, " Dr. Marcia Angell, former editor of The New

England Journal of Medicine, said in an interview with ABC News. " I do think

at a time when a lot of public-health concern is about the national epidemic

of obesity, having a surgeon general who is noticeably overweight raises

questions in people's minds. "

It is not enough, it seems, that the obese must suffer the medical consequences

of their weight, consequences that include diabetes, heart disease, and cancer,

and that cause nearly 300,000 deaths in the United States each year. They must

also suffer the opprobrium heaped on them by people like Angell or Rep.

Sensenbrenner (R-WI), who advised the obese to " Look in the mirror because

you are the one to blame. " In our society, perhaps no group is more stigmatized

than the obese.

The abuse is nothing new, of course. Four hundred years ago, Shakespeare had

Prince Hal hurl a barrage of insults at Falstaff, calling him " fat-witted, "

" horseback-

breaker, " and a " huge hill of flesh. " But Shakespeare had an excuse. In his time

essentially nothing was known about the real reasons that people are fat. Today

we have no such excuse. Modern medical science has gone a long way toward

explaining the causes of obesity, and the bottom line is clear: obesity is not a

personal choice. The obese are so primarily as a result of their genes.

Genetic studies have shown that the particular set of weight-regulating genes

that a person has is by far the most important factor in determining how much

that person will weigh. The heritability of obesity—a measure of how much

obesity is due to genes versus other factors—is about the same as the

heritability of height. It's even greater than that for many conditions that

people accept as having a genetic basis, including heart disease, breast

cancer, and schizophrenia. As nutrition has improved over the past 200

years, Americans have gotten much taller on average, but it is still the

genes that determine who is tall or short today. The same is true for

weight. Although our high-calorie, sedentary lifestyle contributes to the

approximately 10-pound average weight gain of Americans compared to

the recent past, some people are more severely affected by this lifestyle

than others. That's because they have inherited genes that increase their

predisposition for accumulating body fat. Our modern lifestyle is thus a

necessary, but not a sufficient, condition for the high prevalence of

obesity in our population.

Over the past decade, scientists have identified many of the genes that

regulate body weight and have proved that in some instances, different

variants of these genes can lead a person to be fat or thin. These genes

underlie a weight-regulating system that is remarkably precise. The average

person takes in a million or more calories per year, maintaining within a narrow

range over the course of decades. This implies that the body balances calorie

consumption with calorie expenditure, and does with a precision greater than

99.5 percent. Even the most vigilant calorie counter couldn't compete, if

for no other reason than that the calorie counts on food labels are often

off by 10 percent or more.

The genes that control food intake and metabolism act to keep weight in

a stable range by creating a biological force that resists weight change in

either direction. When weight is gained, hunger is reduced. When weight

is lost, the unconscious drive to eat is stimulated and acts to return

weight to the starting point. Moreover, the greater the amount of

weight that is lost, the greater the sense of hunger that develops.

Thus, when the obese lose large amounts of weight by conscious

effort, their bodies fight back even more strongly by increasing

hunger and reducing energy expenditure. If you think it is hard to

lose 10 to 20 pounds (and it is), try to imagine what it would feel

like to lose many tens or even hundreds of pounds.

Anyone who doubts the power of this biologic system should study

the case of a young boy in England a few years back. He had a

mutation in a critical gene, the one that produces the hormone

leptin. Leptin is made by fat tissue and sends a signal informing

the brain that there are adequate stores of energy. When leptin

drops, appetite increases. Because of a genetic error, this boy

could not make this hormone, which left him ravenously hungry

all of the time. At age 4 he ate 1,125 calories at a single meal—

about half of what a normal adult eats in an entire day. As a

result he already weighed 90 pounds and was well on his way

to developing diabetes. At the time, his similarly affected cousin

was 8 and weighed 200 pounds. After a few leptin injections,

the boy's calorie intake dropped to 180 calories per meal, and

by the time he was 6 his weight had dropped into the normal

range. Nothing changed except the hormone levels: his parents

weren't more or less permissive, his snacks did not switch from

processed to organic, his willpower was not bolstered. Rather

this boy was a victim of a malfunctioning weight-regulating

system that led to an uncontrollable drive to eat. This examples

illustrates that feeding behavior is a basic drive, similar to

thirst and other life-sustaining drives. The key role of leptin

and other molecules to control feeding behavior undercuts

the common misconception that food intake is largely under

voluntary control.

While mutations in the leptin gene like the cases described

above are rare, nearly 10 percent of morbidly obese individuals

carry defects in genes that regulate food intake, metabolism,

and body weight. The evidence further indicates that the rest

of the obese population carries genetic alterations in other, as

yet unidentified, single genes or combinations of genes

(polygenes) interacting with environmental factors.

So if you are thin, it might be more appropriate for you to

thank your own " lean " genes and refrain from stigmatizing

the obese. A broad acceptance of the biologic basis of

obesity would not only be fair and right, but would also

allow us to collectively focus on what is most important—

one's health rather than one's weight. There is no evidence

that obese individuals need to " normalize " their weight to

reap health benefits. In fact, it is not even clear whether

there are enduring health benefits to weight loss among

obese individuals who do not suffer from diabetes, heart

disease, hypertension, or liver disease. What is known is

that the obese who do suffer from these conditions

receive a disproportionately large benefit from even

modest weight loss, which together with exercise and a

heart-healthy diet can go a long way toward improving health.

While research into the biologic system that controls

weight is moving toward the development of effective

therapies for obesity, we are not there yet. In the meantime

we must change our attitudes toward the obese and focus

less on appearance and more on health. In their efforts to

lose weight they are fighting against their biology. But they

also are fighting against a society that wrongly believes that

obesity is a personal failing.

M. Friedman, M.D., Ph.D. is the Marilyn M. Simpson

professor and head of the Laboratory of Molecular Genetics

at The Rockefeller University, and an investigator at the

Medical Institute.